This invention relates to a remedial apparatus for use in assisting the breathing of living creatures, and more particularly, to an apparatus useful in cases where the passage of air or other gas to be inspired or expired is obstructed by the inward displacement or collapse of passageway walls of the respiratory system. Such collapse produces uneven distribution of gases through the lungs and affects not only the bulk of gas flow through the airways of the system but also the entire gas exchange process.
For convenience in the following description, reference will be made to the application of the apparatus to human beings. However, it will be understood that suitable forms of the apparatus may be applied to other living creatures. Further, also for convenience, reference will be made to air as the respiratory gas. However, it will be understood that the apparatus may be used with other respiratory gases, for example oxygen and those used in anaesthesia.
For practical purposes, the human respiratory system may be considered as a complex network of visco-elastic tubes branching continuously in decreasing diameter, length, and wall thickness. The different levels are indicated as generations with the trachea as the first, the main bronchi as the second, and so on down to the alveolar sacs as the twenty-third. The trachea and main bronchi are supported by U-shaped cartilages which are joined posteriorly by smooth muscle bands.
Lobar and segmental bronchi (2-4 generation) have fairly firm cartilaginous support in their walls, initially in the form of irregularly shaped plates, and lower down, in the form of helical plates. The small bronchi (5-11 generation) extend through 7 generations with their diameter following from 3.5 to 1 mm. These have no cartilaginous structure.
From the bronchioles until the alveolar sacs (the smallest terminal compartments), the lung paracheyma structure may be represented as randomly oriented flat membranes (septa). In the normal lung, the paracheyma is alwayys in a pre-stretched condition. This creates a sub-atmospheric pressure in the outer surface of the lungs referred to as pleural pressure (Ppl) which maintains the structure expanded. When there is no air flow through the airways, the air pressure within the lungs is constant at all points and the pressure difference across any interior membrane is zero. However, because these membranes are stretched during deformation, a stress exists within them. Lung recoil is due partially to this elastic stretching of the lung paracheyma and partially to surface tension acting throughout the air-fluid interface lining the alveolar sacs.
Alveolar pressure (Palv) is the driving pressure which causes air to flow through the airway in and out of the lungs. To a close approximation, Palv may be considered as made up of two parts; the pleural pressure (Ppl) and the lungs recoil pressure (Pst) so that: EQU Palv=Ppl+Pst
Pst is always positive in sign with respect to the atmospheric pressure and its value is proportional to the lung volume. Ppl is negative for all inspirations and most expirations. During forced expirations, however, Ppl becomes positive in sign due to activity of expiratory muscles. Because Palv is the total pressure drop between the alveoli and the mouth (atmosphere), there is a point within the airways at which the pressure of the air at the inner walls equals Ppl.
At this pressure, Ppl is also the external pressure applied on the airway, the transmural pressure between the inside and the outside of the airway wall will be negative at all points downstream of this point. If the transmural pressure difference is sufficiently strong to overcome the rigidity of the airway, then the bronchi will necessarily collapse.
The above analysis explains why, with a constant lung volume, expiratory flow increases as driving pressure is increased until a critical level is reached and further increase in driving pressure does not result in any increase in expiratory flow.
It has been demonstrated that emphysematous patients exhibiting marked decrease in maximum expiratory flows generate their maximum flows even during quiet breathing. Accordingly, limitation of airflow rate by bronchial collapse is much more marked in such patients. Three combined factors are responsible:
(a) The resistance in the small bronchi of such patients is higher, and therefore the pressure drops more rapidly from the alveoli to the larger bronchi; PA1 (b) The bronchi of an amphysematous person are less able to withstand collapse; and PA1 (c) The recoil pressure in each compartment, (calculated as P=2T/r where T is the elastic tension of the walls and r is the average radius), is reduced because, with the loss of septa, the average radius of the compartments increases.
The above atrophic changes are irreversible and usually progressive. Generally, some respiratory parameters are changed by the chronic obstructive lung disease patient in order to adapt his respiration to his pathologic condition. Firstly, his functional residual capacity (minimum lung volume during quiet breathing) is increased giving rise to the so called barrel chest. By this adjustment, he increases the average diameter of the ducts and the elastic recoil of the lung when the lung is expanded. Bronchial collapse is thereby reduced.
Secondly, the patient learns to increase the expiratory resistance of his upper airways by grunting or pursed-lip breathing. This increase in resistance gives rise to an increase in tracheal pressure which in turn reduces to some extent airway collapse and air trapping in those zones affected by the disease. Nevertheless, pursed-lip breathing also increases the effort requiredn during breathing and leads to a higher oxygen consumption.
Thirdly, the patient tries to avoid making forced expirations such as coughing. The ineffectiveness of the effort can often be more distressing than the limitations of ventilation.
In extreme cases, or during anaesthesia, artificial respiration is used in Chronical Obstructive Lung Disease (C.O.L.D.) patients. Problems of airtrapping and poor gas exchange are frequently encountered in dealing with those patients.
It is one object of this invention to provide an apparatus for increasing airflow during expiration by avoiding or reducing obstruction arising from inward displacement or collapse of the walls of the air passageways.
Another object of the invention is to provide a process for assisting expiration of respiratory gas from the lungs especially but not exclusively during anaesthesia procedures.
Another object of the invention is to provide an apparatus for assisting air flow during expiration by maintaining an outwardly displaced position of gas passageways in the lungs.
Another object of the invention is to improve gas mixing and blood circulation in the lungs.